Intravenous contrast medium is useful to evaluate mediastinal vessels and to identify varices. Administration of oral contrast medium is not routinely needed. In some patients, orally administered positive or negative (water) contrast material can be useful to achieve maximum esophageal distention, helping to differentiate the normal collapsed wall from a thickened wall and an esophageal mass from a mediastinal mass of other origin.

The esophagus extends from the upper esophageal sphincter (cricopharyngeus muscle) to the lower esophageal sphincter, which is at the level of the diaphragmatic hiatus (1). On axial sections, it is seen as an oval or round soft tissue structure, often containing small amounts of intraluminal air. The thickness of the normal esophageal wall is ≤3 mm when the lumen is fully distended and ≤5 mm when the lumen is incompletely distended. The cervical esophagus lies in the midline posterior to the trachea. At the thoracic inlet, the esophagus courses slightly to the left of midline. It then descends to the left of the trachea, posterior to the left main-stem bronchus, and anterior to the descending aorta as it enters the diaphragmatic hiatus (Fig. 8.1) (1,2).

Findings of esophageal pathology are wall thickening, an air–fluid level, a fluid-filled lumen, and increased luminal diameter. These features suggest obstruction, gastrointestinal reflux, or esophageal motility disorder (Fig. 8.2).

Esophageal tumors are rare in children. Those that have been reported include leiomyoma, hamartoma, angiofibromatous polyp, carcinoma, and lymphoma (2,4). On CT, benign esophageal tumors appear as smooth, well-defined, round or ovoid, intraluminal or intramural masses of soft tissue attenuation. The esophageal wall is eccentrically thickened. Multiple leiomyomas have been associated with Alport syndrome (6). CT features of malignant tumors include irregular wall thickening, intraluminal polypoid mass, heterogeneous enhancement, invasion of adjacent soft tissues, regional lymph node enlargement, pleural effusion, and metastases to other organs.

Enlarged paratracheal and subcarinal lymph nodes, secondary to lymphoma, metastases, or infection, such as granulomatous diseases, can extrinsically compress or invade the esophagus (Fig. 8.4). CT findings range from individually enlarged lymph nodes of soft tissue attenuation to a large homogeneous mass obscuring normal fat planes. Esophageal invasion is suggested when there is thickening, spiculation. or ulceration of the wall. The CT appearance of malignant adenopathy is similar to that of adenopathy secondary to inflammation. Clinical correlation and/or biopsy are needed to establish a diagnosis.

Esophagitis in the pediatric population is usually due to gastroesophageal reflux. Other causes include ingestion of caustic agents and oral medications, such as tetracycline or iron sulfate; long-standing foreign bodies; opportunistic infections, usually owing to Candida albicans,
Cytomegalovirus, or herpes virus; and systemic diseases, including Crohn disease, epidermolysis bullosa, graft versus host disease, and Behçet disease (genital and gastrointestinal ulcerations).

CT findings of esophagitis are long-segment, circumferential wall thickening (7). Mild to moderate wall thickening has been associated with reflux esophagitis (Fig. 8.5) and candidiasis, whereas more marked esophageal thickening has been described in Cytomegalovirus infection. A target appearance is seen when there is submucosal edema, which results in a hypoattenuating layer between the enhancing inner mucosa and outer muscularis propria. Esophagitis is easily diagnosed by barium studies or endoscopy. CT is used to detect or confirm the presence of complications, including ulcerations, perforation, and mediastinitis. CT findings cannot be used to predict a specific cause of esophagitis, and clinical or laboratory data are needed for diagnosis.

Esophageal varices are usually a complication of portal hypertension and result from reversal of venous flow in the coronary veins into the distal esophageal veins. Less often, they are produced by superior vena caval obstruction, which results in the veins from the head and upper extremity draining into esophageal veins and the azygos vein. The former varices are termed uphill and the latter are termed downhill. On CT, varices appear as brightly enhancing, smoothly marginated, tubular or rounded structures in the periesophageal region (Fig. 8.6). The attenuation is similar to that of venous blood. Findings of cirrhosis and portal hypertension also may be noted.

In otherwise healthy children, swallowed foreign bodies lodge in the pharynx, proximal to the cricopharyngeal sphincter, or at the level of the thoracic inlet. In patients who have undergone repair of esophageal atresia, they lodge in the proximal esophagus at the site of surgical anastomosis. Plain radiographs and barium studies often suffice to establish the diagnosis. However, these studies are less likely to demonstrate small or only slightly radio-opaque foreign bodies. CT can readily show such foreign bodies (Fig. 8.7), as well as complications, such as esophageal perforation (Fig. 8.8) (8).

Achalasia is associated with absence or degeneration of the myenteric plexus of the distal esophagus. As a result, the lower esophageal sphincter fails to relax, causing distal obstruction. CT findings include a dilated, fluid- and food-filled esophagus (Fig. 8.2). Wall thickness is usually normal.

Esophageal perforation may result from foreign body aspiration, trauma, or instrumentation. Most tears occur in the cervical and upper thoracic esophagus. CT
findings include wall thickening, extraluminal mediastinal air, periesophageal fluid or contrast, and pleural effusion (Fig. 8.8).

Optimal examination of the stomach requires optimal luminal distention, as a collapsed gastric wall can mimic focal or diffuse wall thickening or obscure pathology. Administering positive oral contrast agent or negative contrast material, such as water or effervescent crystals (9,10,11), or positioning the patient in the prone position can help to ensure full gastric distention. Water used as a negative contrast agent is particularly valuable to improve visualization of the underlying gastric mucosa. Lesions of the gastric antrum, anterior wall, and lesser curvature are usually best seen when the patient is scanned in the supine position. The gastroesophageal junction, posterior gastric wall, and greater curvature are often better seen with the patient prone. After administration of intravenous contrast agent, scans are obtained in the portal venous phase of enhancement.

The stomach extends from the esophagogastric junction to the pylorus. The major regions of the stomach are the fundus (most proximal part), corpus (body), and antrum
(most distal part). The right side of the stomach is called the greater curvature and the left the lesser curvature. The stomach contains distinct folds called rugae, which appear thickest in the area of the greater curvature. The thickness of the normal gastric wall and rugal folds ranges between 3 and 5 mm. A thickness >5 mm is abnormal when the stomach is well distended (12). The gastric wall is usually homogeneous. The mucosa commonly shows bright enhancement following administration of intravenous contrast material.

Lesions arising in structures adjacent to the stomach can cause extrinsic deformity or displacement of the stomach. Causes of extrinsic abnormality include splenic enlargement, retroperitoneal neoplasms, such as Wilms tumor or neuroblastoma, an enlarged left hepatic lobe owing to tumor or cirrhosis, and pancreatic pseudocyst.

Trichobezoars (hair) are more common lesions in childhood than phytobezoars (vegetable matter). Phytobezoars are usually seen in older patients. Gastric bezoars present as an epigastric mass or tenderness, vomiting, early satiety, and weight loss. CT findings are a heterogeneous, intraluminal, soft tissue mass containing a mottled air pattern (19) (Fig. 8.12). Administration of water can be useful in confirming an intraluminal location.

Helicobacter pylori infection, eosinophilic gastritis, tuberculosis, Crohn disease, and chronic granulomatous disease of childhood (20) are causes of gastric wall and rugal fold thickening. The fold thickening is usually <1 cm and commonly involves the antrum. Fold thickening may be easier to appreciate if the stomach is distended with water rather than opaque contrast material. Associated findings of hepatic or splenic abscesses support the diagnosis of chronic granulomatous disease of children, whereas concomitant abnormality of the terminal ileum is suggestive of Crohn disease or tuberculosis.

Marked diffuse fold thickening is seen in Zollinger– Ellison syndrome and Menetrier disease. Zollinger– Ellison
syndrome is characterized by increased gastric acid secretion secondary to a gastrinoma, which is a neuroendocrine tumor. CT findings include diffuse gastric wall and rugal fold thickening, ulcerations, and a large volume of fluid in the stomach and bowel related to hypersecretion of acid (Fig. 8.13). A pancreatic mass and hepatic metastases may be seen. Menetrier disease can have marked rugal thickening, but it is not associated with hypersecretion and it spares the antrum.

Hiatal hernia is a protrusion of a part of the stomach into the thorax. There are four types of hiatal hernias. Type I, the most common, is a sliding hernia (gastroesophageal junction displaced into chest) (Fig. 8.14A). Type II is a paraesophageal hernia (gastroesophageal junction below the esophageal hiatus and gastric fundus and sometimes body above the hiatus next to the esophagus). Type III has findings of both types I and II hernias (gastroesophageal junction, fundus, and body displaced into chest), and type IV is an intrathoracic stomach that is associated with herniation of other organs into the chest (21).

Nissen fundoplication is the surgical procedure to treat hiatus hernia and gastroesophageal reflux disease (GERD). In fundoplication, the fundus of the stomach is wrapped around the inferior part of the esophagus. On CT, a fundoplication appears as a soft tissue mass at the gastroesophageal junction (Fig. 8.14B).

Gastric varices may be seen in the setting of portal hypertension or splenic vein thrombosis. CT findings include brightly enhancing, round or serpentine structures within the gastric wall, usually the fundus, or within the associated mesentery or omentum. These are best seen when water is used as a contrast agent and scans are acquired during the portal venous phase of enhancement. Gastric varices without esophageal varices are characteristic of splenic vein thrombosis.

Blunt abdominal trauma can result in gastric perforation, with pneumoperitoneum, hemoperitoneum, interruption of the gastric wall, and leakage of oral contrast medium seen on CT (22). Rupture of the left hemidiaphragm can result in herniation of the stomach into the chest.

Administration of oral contrast medium 45 to 60 minutes before imaging provides adequate opacification of most of the jejunum and ileum. Ingestion of additional contrast material 10 to 15 minutes prior to imaging is helpful to opacify the stomach, duodenum, and proximal jejunum. Positive contrast agent provides good visualization of the bowel lumen, but it may obscure visualization of mucosal lesions. Water used as a negative contrast agent may help to improve visualization of the underlying mucosa. Scanning during the portal venous phase of contrast enhancement usually provides adequate visualization of the small bowel mucosa. Multiplanar reformations and three-dimensional imaging can be helpful in assessing the level of bowel obstruction and longitudinal extent of inflammatory and neoplastic disease (23,24).

The duodenum extends from the pylorus to the duodenojejunal junction at the ligament of Treitz. It has four parts. The duodenal bulb (first portion) is intraperitoneal and lies posterior or posterolateral to the gastric antrum. The descending (second) portion courses caudally to the right of the pancreatic head; it then turns to the left where it enters the retroperitoneum. The horizontal (third) part crosses posterior to the superior mesenteric vein and artery and anterior to the inferior vena cava and aorta. The ascending (fourth) part ascends just left of the superior mesenteric artery to the ligament of Treitz, where it exits the retroperitoneum and becomes the intraperitoneal jejunum.

The small bowel extends from the ligament of Treitz to the ileocecal valve. Jejunal loops have a feathery appearance, containing fine, smooth, linear folds, termed valvulae conniventes. Ileal loops are typically featureless (Fig. 8.15). Normal bowel wall thickness usually does not exceed 3 mm (25). The normal luminal diameter does not exceed 2.5 cm.

The small bowel mesentery connects the jejunum and ileum to the posterior abdominal wall. It appears as a fat-containing area central to the small bowel loops. The superior mesenteric artery (SMA) and superior mesenteric vein (SMV) and their branches and tributaries can be identified on contrast-enhanced CT scans (see Chapter 7). In normal individuals, the SMA lies to the left of the SMV (Fig. 8.15). Abnormalities of bowel rotation are suggested when the relationship of the SMA and SMV is reversed (26,27,28). Mesenteric lymph nodes are not commonly seen on CT scans in infants and children, although nodes ≤5 mm may sometimes be seen in adolescents.

Primary small bowel tumors are uncommon in children. When they occur, they are more likely to be malignant than benign. Patients with small bowel neoplasms come to clinical attention because of a palpable abdominal mass, abdominal pain, small bowel obstruction, or gastrointestinal bleeding. CT is useful in demonstrating extramural tumor extent, invasion of adjacent structures, and adenopathy.

Polyps are the most common benign tumor of the small bowel in children (4). They can be isolated or they may be associated with the multiple polyposis syndromes, such as Peutz–Jeghers (Fig. 8.19), Cronkhite–Canada, and Gardner. When they are large, they are easily recognized on CT, appearing as well-circumscribed, intraluminal soft tissue masses with smooth margins.

Hamartomas, leiomyomas, GISTs, and hemangiomas are rare benign neoplasms of the small intestine in children. Hamartomas and leiomyomas are usually spherical, smooth, homogeneous masses with a predominant extraluminal component. Leiomyomas may contain amorphous calcification and tend to enhance following administration of intravenous contrast material. GISTs have an appearance similar to those in the stomach, appearing as large, exophytic soft tissue masses, which often have low-attenuation areas from necrosis or cyst formation (31). Gastrointestinal hemangiomas may be solitary or diffuse. CT shows focal or diffuse wall thickening and intense enhancement following contrast administration (32,33).

Lymphoma is the most common small bowel malignancy in children and is more often due to non-Hodgkin
lymphoma than to Hodgkin lymphoma. Non-Hodgkin lymphoma typically occurs in the terminal ileum and its mesentery. CT findings of small bowel lymphoma include circumferential bowel wall thickening (>1-cm diameter), a polypoid mural mass, and bulky mesenteric lymph node enlargement (Fig. 8.20) (34). The infiltrated bowel wall has soft tissue attenuation and shows only minimal enhancement. Ulceration, aneurysmal dilatation of the bowel lumen secondary to mucosal infiltration and excavation, and intussusception are common. A mantle of enlarged lymph nodes may envelop the superior mesenteric vessels, producing the sandwich sign.

An increased incidence of lymphoproliferative disorder and B-cell lymphoma has been reported in solid organ transplant recipients (35,36). The CT appearance of posttransplant lymphoproliferative disorder and lymphoma in the immunocompromised host is indistinguishable from lymphoma in the immunocompetent host (Fig. 8.21). However, extranodal involvement, including brain, bone marrow, abdominal viscera (spleen and liver), and mucocutaneous sites, are more frequent in patients with transplant-related lymphoma (35,36).

Leiomyosarcoma has been described in children 4 years of age and older. Adenocarcinoma has been reported occasionally in childhood and usually is far advanced at diagnosis. The CT findings of both tumors include focal wall thickening, a polypoid mass, and an annular stricture with mural thickening (24). Partial or complete bowel obstruction is common. Regional lymph nodes may be enlarged.

The diagnosis of small bowel obstruction is usually established by clinical history, physical examination, and plain abdominal radiography. CT can aid in determining the location and cause of the obstruction when conventional imaging studies are indeterminate (61,62,63,64,65,66,67,68,69,70). There are numerous causes for small bowel obstruction, but the more common causes are intussusception, inguinal hernia, appendicitis, superior mesenteric artery syndrome, and adhesions.

Bowel obstruction can be diagnosed on CT when there are dilated fluid or contrast-filled loops of bowel proximal to a transition zone, beyond which the small bowel and/or colon are collapsed (Fig. 8.30). In the setting of adhesions, beaklike narrowing may be seen at the site of obstruction (71). The sensitivity of CT for detecting small bowel obstruction ranges from about 65% to 100% (64,65,66). The highest sensitivities have been reported in high-grade or long-standing obstruction (61,68). False-negative diagnoses occur in low-grade partial or early obstruction.

In partial obstruction, the small bowel may be minimally dilated and the transition zone may be barely apparent or not seen (64,69). The bowel distal to the obstruction is not completely collapsed, and the colon is normal or minimally dilated and contains fluid and gas. Ileus has a CT appearance similar to that of partial small bowel obstruction.

Closed-loop obstruction refers to the occlusion of a segment of bowel at two points, blocking ingress and
egress of bowel contents. In this scenario, there is eventually compromise of arterial blood flow, leading to ischemia and ultimately infarction (i.e., strangulated bowel). Closed-loop obstruction is most commonly due to midgut volvulus or adhesive bands and less often to internal hernias. CT findings include a distended, U-shaped, fluid-filled loop of bowel, two adjacent collapsed loops of bowel at the site of obstruction (Fig. 8.31), a beaklike appearance of the segments of bowel entering and exiting the closed loop, a whirled or twisted configuration of the bowel near the site of obstruction, and dilated and stretched mesenteric vessels converging toward the site of obstruction (72). Bowel wall thickness is normal.

CT signs of ischemia or strangulation include thickened bowel wall, dilated mesenteric vessels, increased attenuation of the mesenteric fat owing to hemorrhage, pneumatosis intestinalis, gas in portal and mesenteric veins, and ascites (69,71,72). The bowel wall can have a layered appearance resulting from contrast enhancement of the mucosa and muscularis layers with an intervening hypoattenuating layer resulting from submucosal edema, or it may show poor or absent enhancement following intravenous contrast administration.

Administration of oral contrast agents well in advance of the CT study usually serves to opacify the colon and rectum. Rectal contrast, either positive or negative (water or air), can help to clarify suspected colonic pathology but is usually not necessary for a diagnosis. Administration of intravenous contrast agent can be helpful in evaluating causes of wall thickening and mural lesions. Scanning is performed during the portal venous phase of contrast enhancement.

CT colonography is being used to evaluate colonic pathology in adults, but experience with this technique is still limited in children (111). CT colonography requires a bowel preparation similar to that used for conventional colonography. A rectal tube is inserted and the colon is insufflated with room air or carbon dioxide. The colon is scanned with the patient both supine and prone using narrow collimation, a reconstruction interval of 1 mm, and a low-dose technique. Two-dimensional axial and 3D volume-rendered images, including “fly-through” views, are acquired and viewed on a computer workstation. The role of CT colonography in children has been in polyp detection (Fig. 8.44).

The colon extends from the cecal tip to the anus. The ascending and descending colon are retroperitoneal, whereas the transverse and sigmoid colon are intraperitoneal. The colon is easily recognized by its location and its haustral markings when distended by contrast or air. Inherent fecal material also serves as identifier of the colon and rectum. On CT, the thickness of the wall of the colon should not exceed 3 mm (12).

Several variations in colonic anatomy need to be recognized so that they are not mistaken for pathology. The transverse colon may ascend more superiorly than usual, lying anterior and superior to the liver, or it may descend more caudally into the pelvis. Part of the right or left colon may fill the evacuated renal fossa in patients who have renal agenesis or a nephrectomy.

Colonic duplication cysts constitute 15% to 20% of all gastrointestinal tract duplications (3). Clinical findings include a palpable mass, bowel obstruction, and rectal
bleeding. Like other gastrointestinal duplications, most are spherical, low-attenuation masses with thin walls (Fig. 8.45). They usually arise near the cecum and do not communicate with the colonic lumen. In some cases, the duplication is tubular, rather than spherical, and may involve a long segment of the colon or the entire colon. Unlike spherical duplications, tubular duplications can communicate with the lumen.

Congenital anorectal malformation, also known as imperforate anus, is characterized by an abnormal termination of the hindgut. Prior to surgical intervention, CT has been used to show the relationship of the intestine to the levator sling and the amount of residual muscle mass. In cases of postoperative incontinence, CT scans can demonstrate the position of the pulled-through rectum within the levator sling (Fig. 8.46) (112).

In nonrotation of the bowel, the entire colon lies in the left abdomen. In reverse nonrotation, the entire colon is on the right and in incomplete rotation, the cecum is high and near the midline.

Colonic tumors are usually detected on barium studies or at colonoscopy. CT can be useful to further characterize a mass and determine its extent. Juvenile polyps are the most common benign neoplasm of the colon in children. They are inflammatory and not adenomatous as they are in adults and are thought to represent mucus-retention cysts that develop when the orifices of the mucus glands are blocked. Rare benign tumors include lipomas, neurofibromas, and hemangiomas. Colonic polyps appear as well-defined pedunculated intraluminal masses or as sessile masses of soft tissue attenuation (Fig. 8.44). Lipomas have a typical fatty appearance on CT. Neurofibromas present as focal soft tissue masses, whereas hemangiomas are usually intramural nodules in the rectal wall that enhance after intravenous contrast administration.

Malignant neoplasms include lymphoma, adenocarcinoma, and carcinoid (neuroendocrine carcinoma) (113,114). Lymphoma produces marked bowel wall thickening, often >3 cm in diameter. Typically, colonic lymphoma is homogeneous, although large tumors may show low-attenuation areas representing necrosis. The bowel lumen is usually normal or dilated at the site of tumor involvement. Unlike adenocarcinoma, luminal narrowing and bowel obstruction are uncommon. Colonic lymphoma is often associated with mesenteric or retroperitoneal lymphadenopathy. In patients with AIDS, cytomegalovirus infection can cause a focal mass indistinguishable from that seen in patients with lymphoma (115).

CT findings of adenocarcinoma include circumferential or eccentric wall thickening and an irregular or polypoid mass (Fig. 8.47). Luminal narrowing and bowel obstruction are common. Other findings include tumor extension into adjacent organs or the pericolonic fat, mesenteric lymph node enlargement, omental or mesenteric masses, and ascites. Liver and lung are common sites for metastases.

Carcinoid tumors arise from neuroendocrine cells in the mucosa of the bowel and are often small. Most tumors are found in the appendix (114). They may present as a primary colonic mass, but more often they are occult and present with metastatic spread to the mesentery or liver.

Cystic fibrosis is an inherited disease characterized by a generalized dysfunction of the exocrine glands. Gastrointestinal complications occur in 85% to 90% of patients, and the most common of these are meconium ileus, fibrosing colonopathy, and meconium ileus equivalent syndrome. The first two complications occur predominantly in neonates and young children who present with abdominal distention and small bowel obstruction. Meconium ileus equivalent syndrome has a predilection for adolescents and young adults who usually present with acute or chronic abdominal pain, constipation, and a palpable right lower quadrant mass. In most cases, plain abdominal radiographs and barium enema examinations suffice for diagnosis. In some cases, the clinical findings may mimic those of an acute abdomen and CT may be the initial imaging study of choice (126,127). CT findings include colonic wall thickening (mean thickness, 6.4 mm), the accordion sign, pericolonic soft tissue stranding, increased pericolonic fat, and mesenteric lymphadenopathy (Fig. 8.54). The disease involves the cecum and ascending colon in continuity, with variable distal extension. Sinus tracts, fistulae, abscesses, and extensive small bowel involvement are not typical of meconium ileus equivalent syndrome and help to differentiate it from Crohn disease (126,127).

Hemolytic uremic syndrome is a disorder characterized by a prodrome of bloody diarrhea followed by acute renal failure, hemolytic anemia, and thrombocytopenia. The cause is thought to be an antigen–antibody reaction to bacterial toxins, E. coli serotype O 157:H7 being one of the most frequent pathogens. This serotype produces a verotoxin, resulting in a vasculitis which in turn causes deposition of fibrin thrombi in the microvasculature of the kidneys and other organs. Shigella, Salmonella, Campylobacter, Yersinia, and enteroviruses also have been implicated as causes of the hemolytic uremic syndrome. CT findings include colonic wall
thickening, which may be homogeneous or show a layered appearance; pericolonic soft tissue stranding; and ascites (Fig. 8.55) (128). The edematous kidneys may have a lower attenuation value than normal on unenhanced CT scans.

Colonic edema can occur in the setting of cirrhosis and portal hypertension. It usually affects the ascending colon (129).

Perirectal abscesses usually are associated with Crohn disease (Fig. 8.49). Other causes include perforation owing to foreign body or trauma and leakage at a site of surgical anastomosis.

Pneumatosis intestinalis refers to the presence of gas in the wall of the colon and/or small bowel. It is most often associated with bowel necrosis, usually owing to necrotizing colitis of infancy, but it also may be seen in more benign conditions. Benign causes include (a) increased mucosal permeability, related to steroid therapy, immunosuppression, chemotherapy, or graft versus host disease; (b) mucosal disruption related to Crohn disease, ulcerative colitis, or endoscopy; and (c) pulmonary diseases, such as asthma, cystic fibrosis, or mechanical ventilation. On CT, pneumatosis may have a cystic appearance, appearing as well-defined round air collections in the subserosal area of the bowel, or a linear appearance manifesting as streaks of gas within and parallel to the bowel wall (Fig. 8.56). Cyst rupture may result in a benign pneumoperitoneum.